cardiovascular Flashcards
how many people die from cardiovascular disease (CVD) in UK each year
180,000
1 in 3 of all deaths
82,000 coronary heart disease (CHD)
49,000 stroke
someone has a heart attack every 6 minutes
how much blood does the heart pump out?
how much a day?
each side pumps 5 litres per min
7000 litres
how much does the human heart weigh?
200 to 425g
heart structure
vena cava RA tricuspid valve RV pulmonary valve pulmonary artery lungs pulmonary veins LA mitral valve (bicuspid) LV aortic valve aorta
which part of the heart do we refer to when saying systole and diastole?
left ventricle
systole
diastole
contraction
70ml blood from each ventricle
lasts 300ms
relaxation permits filling of heart
550ms at 70beatspermin
filling during first 100-200ms
when does the aortic valve open?
when ventricular pressure higher than in aorta
then closes when ventricular pressure lower than aortic
dichrotic notch
gap on graph between lines of ventricular and aortic pressure
back pressure comes back and shuts valve
closing valves makes heart sounds
1st - mitral valve
2nd - aortic valve
3rd - rare, if disorder, galloping, valve shuts inside out
average heart rate at rest
70 beats per min
blood from atria to ventricles
mainly by gravity but last 20% filling is by atrial contraction
isovolumetric ventricular contraction
early systole during which the ventricles contract with no corresponding volume change
all heart valves are closed
pacemakers
more than 1 in the heart but SA is the quickest so main one
conduction pathway
SA node
AV node
Bundle of His
Purkinje fibres
ionic movement causing pacemaker potential
sodium and calcium influx
reduction in permeability of potassium
phase 4 depolarisation in ventricular myocytes
why refractory period during AP
because needs to take more blood in, can’t always be contracted or blood own’t be able to enter and be pumped
need plateau phase so 1 action potential occurs for 1 contraction
myocytes
muscle cells with single nucleus
cylindrical
often branched with intercalated discs so electrically coupled (connexins)
striated
P
QRS
T
atrial depolarisation
initiates ventricular contraction
also atrial repolarisation
ventricular repolarisation
RR interval
length between 2 R peaks
ECG recording linked to systole and diastole?
systole - QT interval
diastole - RR-QT
tunica intima
tunica media
tunica adventitia
endothelium, supporting conncective tissue, release of paracrine signals
elastic tissue, smooth muscle
external, collagen
arteries are compliant
volume increases with pressure
they stretch so in systole, more blood flows in than out
arterial pressure never reaches 0 so continuous flow (pulsatile rather than intermittent)
Windkessel effect
elastic tissue can accept more blood, and compress back so force blood to move
resistance of flow depends on 3 factors
length of blood vessel - longer = greater resistance
viscosity - lots solute = more resistance
radius of blood vessel
how to alter resistance of blood flow
change radius because can’t change other 2 factors
can restrict lumen
blood flow is laminar
layers of fluid move over each other so flow fastest at centre and slowest at sides because friction from walls
resistance and flow equation
R - resistance
η - viscosity
l - length
r - radius
control of access to the microcirculation
constrict by closing precapillary sphincters to alter resistance and alter flow to certain areas
so stop flow to muscles not in use
anastome - direct line between artery and vein
capillary exchange equation
P - permeability coefficient
A - area of exchange
Ci - Co - conc. gradient
J - flux
oncotic pressure
osmotic pressure exerted by proteins
extracellular fluid has 2 compartments
plasma and interstitial fluid
equilibrium between these in terms of volume
capillaries determine the equilibrium between plasma and interstitial fluid
hydrostatic pressure
colloid osmotic pressure/oncotic pressure
loss of fluid from plasma
reabsorption of fluid into plasma
lymphatic vessels
interwoven between blood vessels so take sup fluid not reabsorbed
no pressure in lymphatic system - have valves
venous return
muscle pump enhances it and puts pressure on valve
always moving towards heart
which parts of the ANS controls heart and blood vessels?
heart - parasympathetic and sympathetic
blood vessels - only sympathetic
positive chronotropic effect
negative chronotropic effect
sympathetic speeds up heart by noradrenaline
parasympathetic slows heart by acetylcholine
sympathetic activity makes….
parasympathetic…
pacemaker potential steeper
threshold hits quicker
makes more shallow, hits threshold later, less beats
how does the sympathetic system increase contractility of myocardium?
action of NA enhancing calcium release in myocytes
positive inotropic effect
increase in contractility
by sympathetic
shifts Starling’s law graph upwards (increased work for each filling pressure)
para- doesn’t change contractility
cardiac output
amount of blood moving through the system
move more blood - increase blood pressure
total peripheral resistance
less volume for same amount of blood - more pressure
determined by radius of vessels
MAP
mean arterial blood pressure
2/3 diastolic pressure and 1/3 systolic pressure
baroreceptors
reads pressure
mainly in aortic arch - carotid artery (where left ventricle pumps blood out so highest pressure)
what determines blood pressure?
cardiac output - depends on heart rate, stroke volume - contractility and filling pressure - venous return
TPR - diameter
renin
less flow detected and secretes renin
converts angiotensinogen to angiotensin I
ACE converts to angiotensin II (lung express a lot of ACE)
angiotensin II
best vasoconstrictor
increase peripheral resistance
increase venous tone
increase cardiac output
secretino of aldosterone - increase retention of Na, increase thirst so increase input and plasma volume, increase ECF and plasma volume - increases filling pressure
atrial stretch receptors
sense filling pressure
reduce ECF and blood volume
ANP
atrial natriuretic peptide
stimulated by atrial stretch receptors, stop from stretching too much
renal excretion of Na and reduces blood volume
sends info to hypothalamus - decrease secretion of ADH - stop releasing water to kidney, stop losing water
what happens to blood flow after cutting off circulation for few minutes?
huge jump up in flow and slowly comes down
adenosine released during hypoxia and causes vasodilation to increase O2 and blood flow
things that cause vasoconstriction
sympathetic tone
angiotensin II
ADH
things that cause vasodilation
adenosine
potassium
NO
adrenaline
haemorrhage
rapid loss of blood
need to maintain blood pressure or will get organ death
need to alter peripheral resistance and volume of vessels
reabsorb extracellular fluid to replace blood but lose viscosity because of this
adrenaline’s effect on vessels
bind to alpha receptors and cause constriction
beta receptors in skeletal muscles
adrenaline cause dilation
heart during exercise
if filling pressure becomes very large, cardiac output fails
stroke volume no longer increases with increasing filling pressure
so don’t overstretch heart muscle because can’t recover pulled muscle in heart, can’t rest it
so change heart rate not stroke volume (reduce time stretching so don’t overstretch)
myoglobin
really good at holding O2 (70%)
low oxygen levels result in
vasoconstriction
